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Acute Fulminant Hepatic Failure, Encephalopathy and Early CT Changes

Published online by Cambridge University Press:  23 September 2014

Sathees Waran Thayapararajah ,
Irene Gulka ,
Ahmed Al-Amri ,
Sujut Das  and
G. Bryan Young
Sathees Waran Thayapararajah
Affiliation:
Department of Clinical Neurological Sciences, University of Western Ontario, London, Ontario, Canada
Irene Gulka
Affiliation:
Department of Clinical Neurological Sciences, University of Western Ontario, London, Ontario, Canada
Ahmed Al-Amri
Affiliation:
Department of Clinical Neurological Sciences, University of Western Ontario, London, Ontario, Canada
Sujut Das
Affiliation:
Department of Clinical Neurological Sciences, University of Western Ontario, London, Ontario, Canada
G. Bryan Young*
Affiliation:
Department of Clinical Neurological Sciences, University of Western Ontario, London, Ontario, Canada
*
Room B10-106, Department of Clinical Neurological Sciences, University Hospital, 339 Windermere Road, London, Ontario, N6A 5A5, Canada. Email: bryan.young@lhsc.on.ca
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Abstract:

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Background:

Acute fulminant hepatic failure (AFHF) is common in tertiary care centres with transplant facilities. Cerebral edema frequently threatens the lives of such patients. We reviewed our cases of AFHF, noting the incidence of cerebral edema with serial CT scans and factors associated with mortality.

Methods:

Patients were captured through HmRI classification of acute liver'hepatic failure. Chart review included tabulation of: demographics, INR; serum bilirubin, creatinine, albumin; in-hospital mortality. Computed tomogram (Ct) scans were re-read with blinding to clinical information and catalogued for changes in sulcal markings, ventricular size and grey-white differentiation (GWD). Inclusion criteria: age equal to or greater than 16 years, encephalopathy, hepatic failure within eight weeks of onset of liver disease, CT scans of head performed.

Results:

Of our 25 cases with AFHF, acetaminophen toxicity was the most common etiology (nine cases). Twelve of the 25 patients (48%) had cerebral edema on CT, including eight of the nine (89%) with acetaminophen toxicity. Decrease in sulcal markings and ventricular size preceded conspicuous alterations in GWD. Fourteen died, including all 12 with cerebral edema, although death was due to herniation in only one patient. None of the hematological or biochemical variables correlated significantly with mortality.

Conclusions:

Acetaminophen toxicity is a common cause of AFHF; this combination has a strong association with cerebral edema. Cerebral edema can be detected in its early stages and followed by baseline and serial CT scans. This facilitates management to prevent fatal brain herniation.

Résumé:

RÉSUMÉ:Contexte:

L'insuffisance hépatique aiguë fulminante (IHAF) est fréquente dans les centres de soins tertiaires qui possèdent des unités de transplantation. L’œdème cérébral met fréquemment la vie de ces patients en danger. Nous avons revu nos cas d'IHAF et noté l'incidence d'œdème cérébral à la tomodensitométrie cérébrale sériée ainsi que les facteurs associés à la mortalité.

Méthode:

Nous avons identifié les patients au moyen de la classification HmRI de l'insuffisance hépatique aiguë. Nous avons relevé dans leurs dossiers les données démographiques, l'INR, la bilirubine sérique, la créatinine, l'albumine et la mortalité hospitalière. Les tomodensitométries ont été relues à l'aveugle quant aux données cliniques et répertoriés selon les changements de la trame des scissures, la taille des ventricules et le contraste entre la substance grise et la substance blanche (CGb). Les critères d'inclusion étaient les suivants : l'âge ≥ 16 ans, l'encéphalopathie, l'insuffisance hépatique survenant dans les 8 semaines suivant le début de la maladie hépatique et une tomodensitométries de la tête.

Résultats:

Chez nos 25 patients atteints d'IHAF, l'intoxication par l'acétaminophène était l'étiologie la plus fréquente, soit chez 9 patients. Douze des 25 patients (48%) présentaient de l’œdème cérébral à la tomodensitométrie, dont 8 des 9 patients (89%) présentant une intoxication à l'acétaminophen. Une diminution des repères des sillons et de la taille des ventricules précédait les altérations évidentes du CGb. Quatorze patients sont décédés dont les 12 patients qui présentaient de l’œdème cérébral. À noter que la mort était due à une hernie du tissu cérébral à travers le trou occipital. Aucune des variables hématologiques ou biochimiques n'était corrélée de façon significative à la mortalité.

Conclusions:

La toxicité à l'acétaminophen est une cause fréquente d'IHAF et est fortement associée à l’œdème cérébral. L’œdème cérébral peut être détecté à un stade précoce de la maladie et le suivi peut être fait par la tomodensitométrie effectuée au début de la maladie et en série par la suite. Ceci facilite le traitement et permet d'éviter une hernie cérébrale fatale.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 40 , Issue 4 , July 2013 , pp. 553 - 557
Copyright
Copyright © The Canadian Journal of Neurological 2013

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